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Published on: September 3, 2016
Protective effect of apocynin on antimycin A-induced cell damage in osteoblastic MC3T3-E1 cells
1Department of Food and Nutrition, Education Graduate School, Kyung Hee University, 1, Hoegi-dong, Dongdaemun-gu, Seoul, 130-701, Korea. cheunmi@hanmail.net
Abstract:
Apocynin is a naturally occurring methoxy-substituted catechol, experimentally used as an inhibitor of NADPH-oxidase. In the present study, we investigated the protective effects of apocynin on antimycin A (AMA)-induced toxicicy in osteoblastic MC3T3-E1 cells. Exposure of MC3T3-E1 cells to AMA caused significant cell viability loss, as well as mitochondrial membrane potential (MMP) dissipation, complex IV inactivation, ATP loss, intracellular calcium ([Ca2+]i) elevation and oxidative stress. Pretreatment with apocynin prior to AMA exposure significantly reduced AMA-induced cell damage by preventing MMP dissipation, complex IV inactivation, ATP loss, [Ca2+]i elevation and oxidative stress. These results suggest that apocynin has a protective effect against AMA-induced cell damage by its antioxidant effects and the attenuation of mitochondrial dysfunction. Apocynin also induced the activation of PI3K (phosphoinositide 3-kinase), Akt (protein kinase B) and CREB (cAMP-response element-binding protein) inhibited by AMA. All these data indicate that apocynin may reduce or prevent osteoblasts degeneration in osteoporosis or other degenerative disorders.
Insights
Apocynin protects osteoblasts from damage by reducing oxidative stress and mitochondrial dysfunction. This natural compound may prevent bone cell degeneration in osteoporosis and other disorders.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Apocynin is a NADPH-oxidase inhibitor.
- Osteoblastic MC3T3-E1 cells are used to study bone cell health.
- Antimycin A (AMA) induces cell damage, including mitochondrial dysfunction and oxidative stress.
Purpose of the Study:
- To investigate the protective effects of apocynin against AMA-induced toxicity in osteoblasts.
- To elucidate the mechanisms underlying apocynin's protective actions.
Main Methods:
- MC3T3-E1 cells were exposed to AMA with or without apocynin pretreatment.
- Cell viability, mitochondrial membrane potential (MMP), complex IV activity, ATP levels, intracellular calcium ([Ca2+]i), and oxidative stress were assessed.
- Activation of PI3K/Akt/CREB signaling pathway was evaluated.
Main Results:
- AMA exposure significantly reduced cell viability and induced mitochondrial dysfunction, ATP loss, calcium overload, and oxidative stress.
- Apocynin pretreatment attenuated AMA-induced cell damage, preserving MMP, complex IV activity, ATP levels, and reducing calcium and oxidative stress.
- Apocynin reversed AMA-induced inhibition of the PI3K/Akt/CREB pathway.
Conclusions:
- Apocynin exhibits protective effects against AMA-induced osteoblast toxicity.
- Its protective mechanisms involve antioxidant properties and the mitigation of mitochondrial dysfunction.
- Apocynin may hold therapeutic potential for degenerative bone disorders like osteoporosis.
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